慢性阻塞性肺病患者心理状况及影响因素

调查慢性阻塞性肺疾病（COPD）患者心理状况和影响因素，对60例患者和60例健康者对照，应用焦虑和抑郁情绪表（HAO）对两组进行问卷调查，结果显示，患者评分显著差于健康者，年龄、病程和通气功能与患者抑郁症状和总分呈显著性相关，提示患者伴有心理障碍，重视和兼顾心理症状诊治颇有必要。     

慢性阻塞性肺病合并肺心病患者生命质量评估

慢性阻塞性肺病合并肺心病患者（肺心病组），与慢性阻塞性肺病患者（慢阻肺组）的生命质量（ＱＯＬ）评分比较，两组呈显著差异。单因素相关分析显示年龄、第一秒用力呼气容积占用力肺活性百分比（ＦＥＶ１／ＦＶＣ％）与肺心病患者ＱＯＬ的各项评分，均呈显著相关性。６分钟距离仅与ＱＯＬ的总均分、日常生活能力评分、社会活动情况评分相关，有统计学意义。提示通过ＱＯＬ测评，不仅可反映肺心病患者病情轻重和影响，同时也说明积     

阻塞性睡眠呼吸暂停低通气综合征患者细胞粘附分子水平的研究

目的探讨细胞粘附分子在阻塞性睡眠呼吸暂停低通气综合症(OS-AHS)发病中的作用。方法应用酶联免疫吸附法(ELISA)检测30例老年OSAHS患者及30例老年健康对照者血清可溶性细胞间粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)和E-选择素的含量。结果OSAHS组血清ICAM-1、VCAM-1、E-选择素含量分别为245.22±71.19ng/ml、24.01±4.79ng/ml、和86.58±48.02ng/ml,均明显高于健康对照组(P<0.01),且随OSAHS程度的加重而明显升高。ICAM-1、E-选择素水平与睡眠呼吸暂停低通气指数(AHI)呈明显正相关(P<0.01);I-CAM-1水平与最低血氧饱和度(SaO2min)呈明显负相关(P<0.01)。结论OSAHS患者血清中可溶性粘附分子ICAM-1、VCAM-1和E-选择素水平可作为反映OSAHS严重程度的敏感指标。     

慢性阻塞性肺疾病急性加重期患者外周血Th17细胞的表达及临床意义

目的 探讨外周血Th17细胞在慢性阻塞性肺疾病急性加重期(AECOPD)患者中的表达及临床意义.方法 以260例慢性阻塞性肺疾病(COPD)患者为研究对象,按临床表现分为COPD稳定期组(130例)和AECOPD组(130例),同时选取50例健康体检者为对照组.采用流式细胞术检测外周血Th17细胞水平,酶联免疫吸附法检测外周血细胞因子IL-17水平,同时检测C-反应蛋白(CRP)及白细胞计数(WBC)水平,记录COPD评估测试(CAT)评分.结果 AECOPD组患者外周血Th17细胞、IL-17、CRP及WBC水平显著高于COPD稳定期组和正常对照组(P＜0.05);经过相应治疗后,AECOPD组患者外周血Th17细胞、IL-17、CRP、WBC水平及CAT评分均较治疗前明显降低,差异具有统计学意义(P＜0.05).相关性分析显示,AECOPD组患者外周血Th17细胞水平与CAT评分呈显著正相关(r=0.91,P＜0.01).外周血Th17细胞水平与炎性因子IL-17也呈正相关(r=0.89,P＜0.01),而AECOPD组患者外周血Th17细胞水平与CRP(r =0.084,P＞0.05)、WBC(r=0.063,P＞0.05)水平无显著相关性.ROC曲线分析显示,外周血Th17细胞水平的曲线下面积(AUC)为0.868(95％ CI0.774～0.918),以外周血Th17细胞水平3.72作为临界值时,其诊断AECOPD的敏感性为88.6％,特异性为86.4％,其显著优于CRP和WBC指标.结论 外周血Th17细胞在AECOPD患者中高表达,其可作为预测COPD急性加重期的有效指标,具有一定的临床运用价值.     

慢性阻塞性肺病和肺心病时血浆心钠素与内皮素的测定

ｐ＜０．０１同肺气肿相比，△ｐ＜０．０１，△△ｐ＜０．０１讨论ＣＰＨＤ早期心功能不全时，ＡＮＦ合成和释放增加，如心脏损伤进一步加重，心房内压明显升高，心房肌血供相对或绝对不足，最后导致心房内ＡＮＦ颗粒减少合成和释放障碍，甚至衰竭，有人发现随心衰程度加重，ＡＮＦ分泌逐渐减少。本研究显示：ＣＰＨＤ组与慢支组及肺气肿组相比，ＡＮＦ升高非常显著，而慢支组与肺气肿组之间相比升高不显著，机理为ＣＰＨＤ由于肾素血管紧张素醛固酮系统的激活，导致水钠潴留，循环血量增多，肺动脉压及右房压力增大，以而导致ＡＮＦ分泌增加，而慢支组及肺气肿组无肺动脉高压，因而升高不明显。ＥＴ主要是由内皮细胞分泌的人体中最强的缩血管物质。已有研究显示心衰越重，升高越明显，随心衰改善，就会下降，本研究进一步揭示，由慢支发展到肺气肿及ＣＰＨＤ，ＥＴ含量存在着显著差异，可能ＥＴ在此一病理过程中起着重要作用，由于ＥＴ收缩肺动脉及支气管动脉，将促进肺气肿与ＣＰＨＤ的发生发展，因而临床上寻找有效的ＥＴ抑制剂，对控制ＣＯＰＤ发展、改善ＣＰＨＤ患者生活质量有重大意义。     

慢性阻塞性肺疾病患者外周血单个核细胞糖皮质激素抵抗的体外观察

慢性阻塞性肺疾病(chronic obstructive pulmonary diease,COPD)是以气道、肺部及全身炎症为特征的疾病,吸烟及有害颗粒的吸入是导致炎症发生发展的主要原因.糖皮质激素是目前常用的治疗COPD的抗炎药物,但临床疗效不满意,可能与COPD组蛋白去乙酰化酶(histone deacetylases,HDACs)活性下降导致的糖皮质激素抵抗有关[1-2].既往的研究表明红霉素可以增加氧化应激下单个核细胞HDAC的活性,并减少NF-κB转录活性及IL-8的合成[3].因此,本实验采用分离的外周血单个核细胞(peripheral blood mononuclear cell,PBMC),建立糖皮质激素抵抗的体外细胞模型,从而为进一步寻找有效的减轻COPD糖皮质激素抵抗的药物及其机制研究提供基础.     

慢性阻塞性肺疾病患者白细胞介素2活性变化的研究

对３５例慢性阻塞性肺疾病患者白细胞介素２（ＩＬ－２）的活性进行测定。结果表明：慢性肺患者急性发作作期ＩＬ－２活性低于缓解期、更显著低于健康人，慢性阻肺各病种间的ＩＬ－２活性，差异均无显著性。     

慢性阻塞性肺疾病和肺心病患者循环内皮细胞变化

慢性阻塞性肺疾病和肺心病患者循环内皮细胞变化广州军区总医院全军呼吸中心（广州５１００１０）彭文鸿邹霞英毛宝龄慢性阻塞性肺疾病（ｃｈｒｏｎｉｃｏｂｓｔｒｕｃｔｉｖｅｐｕｌｍｏｎａｒｙｄｉｓｅａｓｅ，ＣＯＰＤ）和肺心病的发展中均存在肺循环障碍。近年来...     

慢性阻塞性肺病患者动脉血—潮气末CO2分压差与死腔／潮气容积…

对７４例正常人和８５例慢性阻塞性肺病患者研究了动脉血－潮气末ＣＯ２分压差（Ｐａ－ｅｔＣＯ２）和生理死腔／潮气比例（ＶＤ／ＶＴ）的关系。正常人和患者的潮气末ＣＯ２分压（Ｐｅｔ ＣＯ２）均与ＰａＣＯ２密切相关（ｒ分别为０．９０和０．８９，Ｐ＜０．００１），但患者的Ｐａ－ｅｔ ＣＯ２较大，高达２．２１ｋＰａ。正常人和患者的Ｐａ－ｅｔ ＣＯ２均与ＶＤ／ＶＴ呈显著正相关（ｒ分别为０．４８和０．６０，Ｐ均小于     

肺泡巨噬细胞脂质代谢在慢性阻塞性肺病中的研究进展

<正>慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)是一种呼吸道慢性炎症性疾病,高发病率和死亡率造成了巨大社会和经济负担,2019年WHO公布COPD已成为全球第三大死亡原因^[1]。但COPD的发病机制尚不明了。随着脂质代谢研究的深入,在COPD中肺泡巨噬细胞(alveolar macrophage, AM)内的脂质代谢变化也备受关注。Fujii等^[2]在研究中发现了AM中的脂质组成以COPD疾病等级依赖性的方式发生变化,     

Synovial expression of cell adhesion molecules in polymyalgia rheumatica

Polymyalgia rheumatica (PMR) is a common disorder of the elderly: the pathogenesis of the syndrome is still debated, though active synovitis of the shoulder has recently been confirmed. To investigate the pathogenesis of this synovitis we evaluated cell adhesion molecule (CAM) expression in shoulder synovial tissue from patients with PMR, correlated synovial expression with the serum levels of soluble forms, and assessed the changes associated with corticosteroid treatment. Arthroscopic synovial biopsies were obtained from 12 untreated and seven corticosteroid (CS)-treated cases. CAM expression was evaluated by MoAb staining on frozen sections and computerized image analysis. Soluble CAM were quantified by ELISA. Endothelial cells expressed intercellular adhesion molecule-1 (ICAM-l), E- and P-selectins. Infiltrating cells were ICAM-1 and β₁-integrin-positive, while L-selectin expression was limited to intravascular leucocytes. Synovial lining cells strongly expressed vascular cell adhesion molecule-1 (VCAM-1), and less intensely ICAM-1. Only the soluble form of ICAM-1 (sICAM-1) was elevated in untreated patients. CS treatment was associated with a decrease in ICAM-1, VCAM-1 and E- and P-selectin expression. sICAM-1 levels were in the normal range in treated patients. VLA-5 and 6 expression was widely distributed among cell types, and was not CS-sensitive. Active shoulder synovitis is associated with different CAM expression in PMR. ICAM-l expression is widely distributed and correlates with elevated levels of the soluble form; it is significantly lower in CS-treated asymptomatic cases.     

重组sICAM-1对PMA刺激的白细胞与\=肺微血管内皮细胞粘附的影响

目的:探讨重组sICAM-1对大鼠白细胞与肺微血管内皮细胞粘附的影响。方法:采用原代培养的大鼠肺微血管内皮细胞及⁹⁹Tm-HMPAO标记的白细胞,观察不同浓度的sICAM-1、CA7(sICAM-1的单抗)以及sICAM-1·CA7(sICAM-1的二聚体)对PMA刺激的大鼠白细胞与肺微血管内皮细胞粘附的影响。结果:sICAM-1与CA7即使在100mg/L也不能抑制白细胞与肺微血管内皮细胞的粘附,而其二聚体在20mg/L和40mg/L即可抑制42%和50%的细胞粘附(P＜0.05)。结论:sICAM-1对细胞粘附的抑制作用很弱,可能与其单体形式有关。     

肿瘤细胞癌胚抗原的细胞粘附活性研究

本实验对肿瘤细胞系的癌胚抗原(CEA)细胞粘附活性进行了研究。CEA 阳性肿瘤细胞系 LoVo及 HeLa 的单细胞悬液在37℃,RPMI1640全培养基中可以相互粘附而各自形成大小不等的细胞凝团。这种细胞间的粘附不仅可以被抗 CEA 多克隆抗体特异性阻断,而且受到外加 CEA 抗原的竞争抑制。细胞粘附试验也获得了同样结果。实验提示,CEA 为一粘附分子。     

The distribution of adhesion molecules in chronic periaortitis

Chronic periaortitis is a local complication of human atherosclerosis. It is defined as the triad of advanced atherosclerosis, medical thinning and aortic adventitial chronic inflammation. It is present to a variable degree in association with atherosclerotic abdominal aortic aneurysms. These aortic adventitial infiltrates differ from those described solely within the atheroma itself, in that they consist predominantly of B lymphocytes. Many of the lymphocytes are activated and proliferating, and germinal centres are common. In this study, an immunohistochemical analysis was carried out on fresh surgical aortic aneurysm tissue in order to investigate the presence and distribution of activation-inducible adhesion molecules, and to correlate this with the degree of inflammation. A consistent finding was the presence of E-selectin on endothelial cells in up to 50% of the vessels throughout the aortic wall and at the base of the atheroma, independent of the severity of inflammation. ICAM-1 expression was abundant on many cell types and increased with the severity of chronic inflammation, being strongest in the germinal centres. VCAM-1 expression was predominant on follicular dendritic cells and also increased with severity of inflammation. VCAM-1 expression was also detected on vessels within lymphoid follicles. The pattern of expression of the adhesion molecules suggests a role in the initiation and progression of chronic inflammation associated with advanced atherosclerosis.     

Cytokines and cell adhesion molecules associated with high-intensity eccentric exercise

Unaccustomed, eccentrically biased exercise induces trauma to muscle and/or connective tissue. Tissue damage activates an acute inflammatory response. Inflammation requires the effective interaction of different physiological and biological systems. Much of this is coordinated by the de novo synthesis of families of protein molecules, cytokines. The purpose of the present paper was to determine changes in blood levels of various cytokines in response to exercise-induced muscle damage that was effected using high-intensity eccentric exercise. Six healthy, untrained, college-age male subjects were required to perform the eccentric phase of a bench press and a leg curl (4 sets, 12 repetitions/set) at an intensity equivalent to 100% of their previously determined one-repetition maximum. Samples of blood were drawn at the following times: before exercise and 1.5, 6, 12, 24, 48, 72, 96, 120, and 144 h after exercise. These samples were analyzed for interleukins (IL): IL-lβ, IL-6, and IL-10; tumor necrosis factor-α; colony stimulating factors (CSF): granulocyte-CSF, macrophage-CSF, and GM-CSF; for cell adhesion molecules (CAM): P- and E-selectin, and intercellular cell adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1). Results were analyzed using a repeated-measures analysis of variance (P=0.05). Compared to baseline values, IL-1β was reduced (P=0.03) at 6, 24, and 96–144 h after exercise; IL-6 was elevated (P=0.01) at 12, 24, and 72 h after exercise; IL-10 was elevated (P=0.009) between 72 and 144 h after exercise; M-CSF was elevated (P=0.005) at 12 and 48–144 h after exercise; and P-selectin was reduced (P=0.01) between 24 and 144 h after exercise. It is concluded that when high-intensity eccentric exercise is compared to strenuous endurance exercise, post-exercise changes in cytokines do occur, but they are generally of a smaller magnitude, and occur at a later time period after the termination of exercise. Accepted: 28 December 1999     

急性心肌梗塞病人细胞粘附分子与补体激活成分的动态变化

目的:探讨急性心肌梗塞(AMI)病人血浆细胞粘附分子和补体活化成分的变化。方法:采用酶联免疫吸附法(ELISA),检测了67例AMI病人发病第1、4、7d时和38例健康人,42例陈旧性心肌梗塞(OMI)病人白细胞CD18表达、血浆可溶性细胞间粘附分子-1(sICAM-1)、可溶性血管细胞间粘附分子-1(sVCAM-1)和血浆补体活化片段(sC5b-9)浓度的变化。结果:AMI病人白细胞CD18表达、sICAM-1、sVCAM-1和sC5b-9浓度非常显著高于对照组和OMI病人(P＜0.01)。发病第1-7d,白细胞CD18表达、sICAM-1、sVCAM-1和sC5b-9浓度逐渐降低。死亡者和伴有室性心律失常者各指标增高较存活者和无室性心律失常者更明显(P＜0.01)。AMI病人白细胞CD18表达、sICAM-1、sVCAM-1浓度与sC5b-9浓度呈正相关(r=0.648,0.652,0.668,0.698,0.914,0.725,0.737,0.752,0.792,P＜0.01),白细胞CD18表达与sICAM-1、sVCAM-1浓度呈正相关(r=0.662,0.683,0.695,0.738,0.744,0.745,P＜0.01)。结论:细胞粘附分子和补体激活成分的相互作用参与了AMI的发生和发展,且与病情严重程度和预后有密切关系。     

多种粘附分子基因在原发性肝癌的表达及其临床意义

目的:探讨多种粘附分子基因在原发性肝癌中的表达及其临床意义。方法:取64例用RT-PCR法半定量检测肝癌粘附分子的基因表达情况,分析其临床意义。结果:(1)原发性肝癌各粘附分子的表达率分别为:E-钙粘蛋白 90.62%、细胞间粘附分子-1 93.75%、粘附分子CD44 50.00%、粘附分子CD_44V 96.88%、整合素α₅ 100%、整合素β₁ 100%,CD44与其他粘附分子表达率的差异显著。(2)肝癌组织各粘附分子E-钙粘蛋白 、细胞间粘附分子-1 、粘附分子CD44、粘附分子CD_44V 、整合素α₅、整合素β₁ mRNA的表达量分别为:1.24±0.54、0.96±0.37、0.62±0.73、0.86±0.33、 0.97±0.49、1.41±0.24,其中粘附分子CD44与E-钙粘蛋白、整合素β₁的表达量差异显著。(3)肝癌分期与粘附分子基因mRNA表达量的关系显示:E-钙粘蛋白、粘附分子CD44的表达量随分期增高而下降,其中粘附分子CD44Ⅰ-Ⅱ期和Ⅳ期的表达量差别显著;细胞间粘附分子-1、粘附分子CD_44V,整合素α₅、整合素β₁的表达量随分期增高而增高,其中细胞间粘附分子-1Ⅰ-Ⅱ期和Ⅳ期的表达量差别显著。(4)肝癌粘附分子基因mRNA表达量与临床病理生理特点相关分析显示:肝癌粘附分子基因mRNA表达量与肿瘤大小、有无转移、有无包膜和结节数目有关,与AFP水平、肝硬化情况、肝功能状况无关。结论:肝癌粘附分子基因mRNA的表达存在明显的差异,粘附分子CD44表达缺失率高。肝癌粘附分子基因mRNA的表达与肿瘤大小、有无转移、结节数目、有无包膜相关。     

Cyclosporin A reduces expression of adhesion molecules in the kidney of rats with chronic serum sickness

Treatment with cyclosporin A (CsA) improves proteinuria and reduces renal cellular infiltration in chronic serum sickness (CSS). We examined if these effects were associated with a reduced renal expression of CD54 and its ligands, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and MHC class II molecules. We studied two groups of rats in which CSS was induced by daily injections of ovalbumin (OVA): a group treated with CsA (OVA.CsA group, n = 11) and a group that received no treatment (OVA.CSS group, n = 11). An additional group of five rats (control group) received only phosphate buffer. Immunostaining techniques were used to follow CSS and to study the expression of CD54, CD18, CD11b/c, IFN-gamma, TNF-alpha and MHC class molecules. Proteinuria (mg/24 h) was reduced from 248.2 +/- 73.1 (OVA.CCS group) to 14.5 +/- 13.1 with CsA treatment (P < 0.0001). The renal expression of CD54 and its ligands (CD18 and CD11b/c) was reduced by 50% to 75%. Correspondingly, there was a 60% to 85% reduction in the number of infiltrating leucocytes. The number of cells expressing TNF-alpha, IFN-gamma and MHC II molecules was also reduced. CsA reduces expression of CD54 and its ligands. This effect is associated with a reduction of cellular infiltration, IFN-gamma, TNF-alpha-producing cells and with MHC II expression in the kidney. These findings suggest that expression of adhesion molecules plays a critical role in CSS and underline the importance of cellular immunity in this experimental model.     

多发性硬化患者外周血白细胞粘附分子的表达

目的 :探讨多发性硬化 (MS)患者外周血白细胞粘附分子表达的水平及予甲基强的松龙 (MP)治疗后的变化。方法 :流式细胞仪测定 2 8例缓解复发型MS患者及 12例复发期MS予静脉MP治疗后外围血淋巴细胞和单核细胞细胞间粘附分子 3(CD5 0 )、细胞间粘附分子 1(CD5 4 )、整合素LFA 1β亚单位 (CD18)、非常晚抗原 4 (VLA 4 )α、β亚单位 (CD4 9d、CD2 9)和 (- )选择素 (CD6 2L)的阳性百分率。结果 :复发期MSCD4 9d和CD2 9在淋巴细胞和单核细胞、CD5 4和CD6 2L在单核细胞的阳性百分率高于缓解期MS和对照组 ,复发和缓解期MSCD5 4在淋巴细胞的阳性百分率高于对照组 ;MP治疗后 ,CD5 4和CD4 9d在淋巴细胞和单核细胞、CD6 2L在单核细胞的阳性百分率下降。结论 :MS患者外周血白细胞粘附分子的表达升高并可作为MS活动期的指标     

The distribution of adhesion molecules in human atherosclerosis

Chronic inflammatory cells are a recognized component of atherosclerotic plaques at all stages of development. As adhesion molecules play a fundamental role in inflammatory processes, we have carried out an immunohistochemical investigation of the distribution of endothelial leucocyte adhesion molecule-1 (ELAM-1)*, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human atherosclerotic lesions. Autopsy specimens from abdominal aorta and coronary arteries were obtained from 21 cases within 24 h of death. ELAM-1 and ICAM-1 were consistently expressed by the entire intimal endothelium of normal coronary arteries and also by the intimal endothelium overlying aortic fatty streaks. Both coronary artery and aortic lesions showed strong staining for ICAM-1 on and around macrophages. VCAM-1 was not detected on intimal endothelial cells, but strong staining of adventitial lymphoid aggregates for this molecule was seen. This work suggests a role for ELAM-1 and ICAM-1 in mononuclear cell recruitment during atherogenesis.